The overall objective of our research project is to investigate the mechanism of 3-amino-1H,2,4-triazole (AT) induced cataract. We have shown that there is 2-3 fold increase in H2O2 concentration in eye humors as a result of catalase inhibition in iris, ciliary body, retina, lens, and cornea. During our study on the effect of H2O2 on lens we have observed that in AT induced cataract there is a marked inhibition of Na ion,, K ion-activated ATPase of lens, showing the possible oxidative damage to the active sulfhydryl group. It is also found that it is H2O2 which produces decrease in uptake of rubidium and L-proline showing damage to lens plasma membrane. We intend to study in detail the cation transport and amino acid transport in lens. Since active transport is energy is dependent, we will study the effect of AT on anaerobic glycolysis and ATP in lens. We propose to study Glucose-6-phosphate dehydrogenase, 6-phosphogluconic acid dehydrogenase and GSSG-reductase in lens to observe the effect of AT on HMP.We will extend studies involving GSH, GSSG, PSH, ascorbic acid in lens and ascorbic acid and H2O2 in aqueous and vitreous humors in cataract induced by AT in rabbit to measure the antioxygenic capacity of lens. Direct demonstration of H2O2 in lens will be of significance, so we will continue attempts to determine H2O2 in lens.